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Biomedical subjects

J F Goodwin

Publications and source records attributed to J F Goodwin.

At least 19 recordsLinked to original sources
PubMed1979

Antibodies to Coxsackie B viruses in congestive cardiomyopathy.

Fifty patients with congestive cardiomyopathy have been studied for evidence of previous Coxsackie B virus infection and compared with age- and sex-matched controls who had been admitted to hospital for investigation of other cardiac diseases. High neutralisation titres (greater than or equal to 1024) to Coxsackie B viruses were more common among the controls. On subdividing the patients according to their length of symptomatic history before study, high titres were more common only in those with a short history (less than or equal to 1 year). High titres were more common when there had been a febrile illness at the onset of symptoms. Endomyocardial biopsies of 18 patients disclosed no evidence of myocarditis, or, in 12 cases, of viral involvement. Although the evidence remains circumstantial, these results support the theory that Coxsackie B viruses may cause congestive cardiomyopathy and encourage further research into the mechanisms of myocardial cell damage by these visuses.

Adult↗
PubMed1978

Regional left ventricular wall movement in hypertrophic cardiomyopathy.

Left ventriculograms of 20 patients with hypertrophic cardiomyopathy were digitised frame by frame and analysed using a contour display. Abnormalities of regional wall movement were present in 17, and included an abnormal sequence of inward movement during systole (13), regional delay in the onset of inward movement (10), and an abnormal dispersion of peak velocities (5). Diastolic wall movement was disturbed in 13, because of abnormal peak velocities in 7 and regional asynchrony in 6. Abnormal wall movement during the two isovolumic periods was rare in hypertrophic cardiomyopathy, unlike ischaemic heart disease. These disturbances may reflect underlying structural abnormalities.

Cardiomyopathy, Hypertrophic↗
PubMed1978

Left ventricular relaxation and filling in hypertrophic cardiomyopathy. An echocardiographic study.

Echocardiograms showing left ventricular cavity and mitral valve cusps simultaneously were recorded in 36 patients, apex cardiograms being obtained in 26 of them. These were digitised and continuous plots made of left ventricular dimension, its rate of change, and anterior mitral leaflet velocity, and were compared with those in 20 normal subjects. Peak mitral diastolic closure rate was reduced to 120 +/- 80 mm/s, compared with normal (250 +/- 60 mm/s). Peak rate of increase of dimension was normal (13.4 cm/s), though the pattern of filling was disturbed, with the duration of rapid filling prolonged in 5, and shortened in 15, suggesting restriction. Mitral valve opening, normally synchronous with minimum dimension, was delayed by a mean of 76 ms, and during this period there was an abnormal increase in dimension. Dimension also increased by 50 +/- 25 per cent of the total diastolic excursion before the 'O' point of the apex cardiogram compared with 21 +/- 7 per cent in normals, and the timing of peak rate of increase of dimension was delayed by 50 +/- 20 ms instead of being synchronous with the 'O' point as normal. None of these findings correlated with the reduction in peak mitral diastolic closure rate. Noninvasive methods thus show that relaxation may be abnormal in hypertrophic cardiomyopathy. Delay in mitral valve opening and disturbances in the rate, duration, and co-ordination of wall movement during filling suggest the presence of segmental abnormalities of left ventricular function.

Adolescent↗
PubMed1978

Left ventricular function in ischaemic heart disease. A review.

The clinical significance of the abnormalities seen at left ventriculography in ischaemic heart disease is discussed. Aneurysms may be recognized when left ventriculography is combined with coronary arteriography to show the characteristic obliteration of the supplying artery. Localized areas of abnormal contraction seen at rest are almost certainly indicative of infarcts. Similar areas provoked by exercise or atrial pacing represent the site of acute ischaemia. The ischaemic ventricle may be recognized by abnormal response to exercise, even in the absence of angina. The abnormal response may be reversed by successful revascularization surgery.

Angina Pectoris↗
PubMed1977

Left ventricular filling in hypertrophic cardiomyopathy. An angiographic study.

In order to study left ventricular filling in hypertrophic cardiomyopathy, left ventricular cineangiograms of 20 patients were digitised frame by frame and compared with those of 10 normal subjects. Peak left ventricular filling rate was 770+/-260 ml s-1 (mean+/-1 standard deviation), not significantly different from normal. Mitral valve opening was delayed, occurring 140+/-40 ms after time of minimum cavity area, compared with 93+/-14 msec in normals (P less than 0-01), indicating abnormal relaxation. Peak left ventricular filling rate was correlated inversely with this delay (r = 0-69, P less than 0-01), which was greater in patients with angina (155+/-27 ms) than in those without (85+/-23 ms) (P less than 0-01). The rapid filling period was also abnormally prolonged in 8 patients. End-diastolic transverse dimension was normal (5-3+/-0-7 cm) but end-systolic dimension was reduced (2-4+/-0-4 cm) (P less than 0-01) because of abnormal cavity shape. Peak rate of change of dimension during filling (18-7+/-5-3 cm s-1) was greater than normal (11-3+/-3-9 cm s-1) (P less than 0-01), and correlated with peak filling rate (r = 0-82, P less than 0-001). Thus, peak filling rate is normal in hypertrophic cardiomyopathy, but the filling pattern may be abnormal, apparently because of impaired relaxation and abnormal cavity shape rather than mechanical obstruction to inflow.

Adult↗
PubMed1976

Effect of acute administration of propranolol on ventricular function in hypertrophic obstructive cardiomyopathy measured by non-invasive techniques.

Seventeen patients with hypertropic obstructive cardiomyopathy, were studied using non-invasive techniques before and after the intravenous injection of 5 mg propranolol. The folloeing were analysed: left ventricular ejection time index, derived from the carotid pulse and heart rate; the isovolumic relaxation time, derived from the apex cardiogram and phonocardiogram; the diastolic closure rate of the mirtal valve; and the left ventricular diameters, systolic and diastolic, both measured by echocardiography. Propranolol produced shortening of the isovolumic relaxation time, increase in both the diastolic closure rate of the mitral valve and left ventricular systolic and left ventricular diastolic diameters. These results show that propranolol increases the rate of filling and the volume of the left ventricle, indicating that an improvement in distensibility is produced by beta-adrenergic blockade.

Cardiomyopathy, Hypertrophic↗